*2.1.6 Ocular and systemic inflammation*

Recent studies focus on the significance of inflammation in the developments of DR [32–36]. There is strong evidence that ischemia and retinal hypoxia induce release of VEGF and inflammatory molecules at the level of endothelial and glial cells. Furthermore, several studies support the idea that ocular inflammatory disorders, such as prolonged post cataract surgery healing, uveitis, keratitis, are related to DR progression [32–36].

There are increased evidences that chronic systemic inflammation is also related to increased risk of DR onset and progression. In an experimental animal model, recurrent exposure to systemic LPS leads to injury of capillary endothelium and in vivo thinning of the retina in hyperglycemic mice, but not in healthy controls [37]. There are clinical evidences of increased incidence of DR and PDR in long standing non-healing foot ulcer, that could be explained due to the associated chronic low-grade systemic inflammation [38–42].
